Etiologic and pathogenetic factors in hypertensive crise development among patients with primary arterial hypertension

• Main Authors: V. A. Lusov, E. M. Evsikov, Yu. M. Mashukova, R. A. Sharipov, . .
• Format: Article
• Language: Russian
• Published: «FIRMA «SILICEA» LLC 2008-08-01
• Series: Российский кардиологический журнал
• Subjects: arterial hypertension; crises; hemodynamics; hormonal regulation; renal function and pathology
• Online Access: https://russjcardiol.elpub.ru/jour/article/view/1580
• ISSN: 1560-4071; 2618-7620

To identify the causes and mechanisms of hypertensive crise development in primary arterial hypertension (AH), complex clinical, biochemical, hormonal, hemodynamic and instrumental examination was performed in 563 patients (189 men, 374 women aged 25-66 years) with Stage I-IIIprimary AH(WHO classification, 1997) and hypertensive crises. The control group included 619 patients (207 men, 412 women aged 31-66 years) with crise-free Stage I-III primary AH. Intracardial and central hemodynamics was assessed by echocardiography, tetrapolar rheography, and radiocardiography. Instrumental urologic examination included renoradiography, static and dynamic renal scintigraphy, ultrasound and computed renal and suprarenal tomography, excretory urography, and selective angiography of renal arteries if necessary. Glomerular filtration rate was assessed by endogenous creatinine clearance, and microproteinuria - by urinary excretion of albumin and beta-2-microglobulin. Plasma levels of hypophysis, thyroid, parathyroid, suprarenal and gonad hormones, as well as excretion of FSH, IH, aldosterone, and cyclic nucleotides was measured by radio-immunologic methods. Stressogenic, psychogenic, and neurological factors influenced hypertensive crise development and pathogenesis among more than two-thirds of primary AH patients. Hyperkinetic circulation during the crise was not explained by left ventricular hypertrophy, remodelling, or chronic pathology. Aortal and retinal pathology was more prevalent in crise-free AH patients. Crise AH course was associated with hyper-secretion of hypophyseal gonadotropins and thyrotropin, suprarenal aldosterone, and changes in the ratio of cyclic nucleotides excreted with urine. Renal pathology and dysfunction at complex clinical and instrumental examination was observed in more than two-thirds of AH patients with hypertensive crises, with high prevalence of chronic uni- or bilateral renal inflammation, nephrosclerosis in calices and renal poles. Renal artery stenosis, with uni- or bilateral changes in renogram secretory phases, functioning parenchyma reduction, and increased plasma renin activity, was less prevalent. Disturbed nitrogen-excretory and filtration renal functions were not directly related to hypertensive crise development.